Recurrent Coronary Events Research Articles

Brom Aortoplasty for Supravalvular Aortic Stenosis

Controversy remains regarding the optimal surgical approach for children with supravalvular aortic stenosis (SVAS). Since 1997 we have used Brom three-patch aortoplasty for patients with SVAS. We prefer computed tomography (CT) imaging for preoperative evaluation rather than cardiac catheterization as it avoids the well-known morbidity of general anesthesia. The purpose of this study was to present our intermediate-term results of this strategy. Twenty consecutive patients with SVAS were treated with Brom aortoplasty. Mean age was 3.7 ± 5.9 years (median, 1.5 years). Twelve patients had Williams syndrome. Ten patients had preoperative advanced medical imaging (seven CT, three magnetic resonance imaging) and did not have cardiac catheterization. Mean times for cardiopulmonary bypass and cross-clamp were 172 ± 29 minutes and 110 ± 21 minutes, respectively. Ten patients had simultaneous pulmonary artery stenosis patching. Median length of stay was seven days. There was no operative or late mortality. Mean follow-up was 6 ± 5 years. There were no reoperations on the aortic root. Fifteen patients had mild or less aortic insufficiency (AI) and two had moderate AI. One patient who had infant balloon dilation of the aortic valve and postoperative subacute bacterial endocarditis had moderate-to-severe AI and aortic stenosis (AS). One patient had moderate residual SVAS; all others had no AS. No patients had late coronary insufficiency. Brom aortoplasty promotes restoration of normal aortic root geometry and relief of coronary ostial stenosis, which is important in preventing myocardial ischemia. Computed tomography imaging is our preferred diagnostic modality. Intermediate-term outcomes are excellent with no recurrent SVAS, coronary events, or reoperations on the aortic valve.

Ticagrelor for Secondary Prevention of Atherothrombotic Events in Patients With Multivessel Coronary Disease

BackgroundPatients with prior myocardial infarction (MI) and multivessel coronary disease (MVD) are at high risk for recurrent coronary events. ObjectivesThe authors investigated the efficacy and safety of ticagrelor versus placebo in patients with MVD in the PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin–Thrombolysis In Myocardial Infarction 54) trial. MethodsPatients with a history of MI 1 to 3 years before inclusion in the PEGASUS-TIMI 54 trial were stratified in a pre-specified analysis based on the presence of MVD. The effect of ticagrelor (60 mg and 90 mg) on the composite of cardiovascular death, MI, or stroke (major adverse cardiovascular events [MACE]), as well as the composite of coronary death, MI, or stent thrombosis (coronary events), and on TIMI major bleeding, intracranial hemorrhage (ICH), and fatal bleeding were evaluated over a median of 33 months. ResultsA total of 12,558 patients (59.4%) had MVD. In the placebo arm, compared with patients without MVD, those with MVD were at higher risk for MACE (9.37% vs. 8.57%, adjusted hazard ratio [HRadj]: 1.24; p = 0.026) and for coronary events (7.67% vs. 5.34%, HRadj: 1.49; p = 0.0005). In patients with MVD, ticagrelor reduced the risk of MACE (7.94% vs. 9.37%, HR: 0.82; p = 0.004) and coronary events (6.02% vs. 7.67%, HR: 0.76; p < 0.0001), including a 36% reduction in coronary death (HR: 0.64; 95% confidence interval: 0.48 to 0.85; p = 0.002). In this subgroup, ticagrelor increased the risk of TIMI major bleeding (2.52% vs. 1.08%, HR: 2.67; p < 0.0001), but not ICH or fatal bleeds. ConclusionsPatients with prior MI and MVD are at increased risk of MACE and coronary events, and experience substantial relative and absolute risk reductions in both outcomes with long-term ticagrelor treatment relative to those without MVD. Ticagrelor increases the risk of TIMI major bleeding, but not ICH or fatal bleeding. For patients with prior MI and MVD, ticagrelor is an effective option for long-term antiplatelet therapy. (Prevention of Cardiovascular Events [e.g., Death From Heart or Vascular Disease, Heart Attack, or Stroke] in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin [PEGASUS]; NCT01225562)

Innate Immune Mechanisms in Myocardial Infarction - An Update

Abstract Acute myocardial infarction (AMI) is a disease associated with high morbidity and mortality. Currently there are no available treatments specifically targeting the post-ischemic myocardial processes that lead to heart failure and recurrent coronary events. The innate immune system plays a central role in the two consecutive phases that follow an acute ischemic event: the inflammatory phase and the reparatory phase. The inflamatory phase involves a massive infiltration of neutrophils and inflammatory Ly6Chi monocytes into the injured myocardium. The reparatory phase is orchestrated by reparatory Ly6Clo macrophages that clear necrotic and apoptotic cells through efferocytosis, secrete anti-inflammatory mediators and stimulate fibrosis and repair. Important recent studies provided proof that Ly6Chi monocytes that enter the myocardium in the inflammatory phase upregulate the orphan nuclear receptor Nr4a1 and switch phenotype to Ly6CloNr4a1hi reparatory macrophages. Additionally, neutrophils have been shown to promote cardiac recovery by upregulating expression of the efferocytosis receptor MerTK on reparatory macrophages. A finely tuned balance between the inflammatory and the reparatory phases is thus essential for limiting myocardial damage and promoting efficient recovery. Treatment strategies targeting only the inflammatory phase have so far failed to improve prognosis in AMI patients. A detailed understanding of the interplay between the two phases of the innate immune response is paramount for designing efficient therapies able to improve post- AMI prognosis. In the current review, we summarize the state-of-the-art of the field and discuss previous therapeutic attempts and currently ongoing clinical trials targeting innate immune mechanisms in AMI patients.

A prospective cardiometabolism ApPRoach of mechanisms of coronary plaque rupture to apprehend patients at risk of recurrent events — The APPROACH registry

Despite improvement in management of coronary artery disease (CAD), recurrent coronary events remain frequent. The aim of this study is to assess predictive factors of plaque rupture, leading to an acute coronary syndrome (ACS) by combining metabolic evaluation and coronary plaque imaging. This study involved two cohorts of patients, one concerning stable CAD and one ACS patients. In both groups of patients, plaque imaging was performed with standard coronary angiogram and optimal coherence tomography (OCT) in the 3 main coronary vessels defined by diameter superior to 2.5 mm. Recurrent major adverse cardiac events were collected during follow-up. Comparison of stable and unstable CAD patients will be performed to try to characterize criteria of plaque vulnerability. The preliminary results regarding the ACS cohort are presented in this abstract. We included 48 patients with mean age of 60.5 years and 87.3% of men. A three-vessel atherosclerotic disease was found in 42% of patients. A total of 142 non-culprit coronary lesions were analysed by OCT for a mean run of 60.4 mm by artery and total of 5854 mm. B2/C complex lesions (AHA/ACC classification) were represented in 28.2% of patients. OCT analysis allowed to define coronary lesions with mean distance from ostium of 22.6 mm, mean stenosis length of 11.9 mm and mean minimum lumen area (MLA) of 3.95 mm 2 with 66.1% of patients with MLA < 4mm 2 . Lesions were distributed in 60% of fibro-fatty plaques, 34% of fibro-calcified plaques and 5% of neo-angiogenesis. Systematic plaque characterization on non-culprit lesions found 7 vulnerable thin-cap fibroatheroma plaques and 3 asymptomatic plaque ruptures. OCT analysis of non-culprit coronary lesions is feasible and allows to highlight vulnerable lesions such as asymptomatic plaque ruptures. Analysis of stable cohort, biomarkers and follow-up of patients are necessary to define predictive factors of plaque rupture.

The role of cytokine gene polymorphism in the development of acute myocardial infarction

The continuous growth of cardiovascular diseases is one of the important challenges facing the modern medicine. They are the primary cause of death both in developed countries and inUkrainein particular. The aim of the study is to perform analysis of modern literary sources related to the role of cytokine gene polymorphism in the development of acute myocardial infarction. The basis for the search for candidate genes was study of individual characteristics and identifying genetic polymorphisms that increase the risk of triggering mechanisms of atherosclerotic lesions of the coronary vessels and the consequent acute myocardial infarction development. Cytokine genes feature a very high level of polymorphisms. The obtained results of the study are quite contradictory, in addition there is no consensus on their application. One of these candidate genes is the gene encoding interleukin-6 production. This is one of the proinflammatory cytokines, elevated levels of which are associated with the development and course of coronary heart disease, as well as with the processes of the atherosclerotic plaque destabilization. Polymorphic marker in interleukin-6 (-174-G/C) gene promoter is associated with IL-6 gene expression level and the level of Interleukin-6 inplasma, and can affect the course of ischemic heart disease. The tumor necrosis factor-α is a multifunctional proinflammatory cytokine which is produced mainly by monocytes and macrophages. Concentration of tumor necrosis factor-α in blood plasma is constantly increased in patients after acute myocardial infarction with an increased risk of recurrent coronary events. These data support the hypothesis that stable patients are at risk of constant inflammatory instability. Increased production of tumor necrosis factor-α is considered an important cause of destabilization of atherosclerotic plaques. The gene cluster of tumor necrosis factor-α is within the region of class III genes of highly polymorphic major histocompatibility complex, located on human chromosome 6 at the position 6p21.1–21.3. Another candidate gene encodes interleukin-10, being an anti-inflammatory cytokine is an inhibitor of inflammation located on chromosome 1 at the position 1q31–q32. The research identified a number of IL-10 gene polymorphisms at positions -592, -627, -1082. Conclusions. Analysis of the above literature allows us to make a conclusion that: first, the concentration of cytokines depends on the genetic characteristics of an individual; secondly, cytokine gene polymorphism may be of importance in regard to the course of coronary heart disease.

Homeostatic cytokines interleukin-7 (IL-7) and IL-15 drive the expansion and activation of CD4+CD28null t cells in patients with myocardial infarction

Aim: We have previously shown that CD4+CD28null (CD28null) T cells, a unique T lymphocyte subset with pro-inflammatory and cell-lytic phenotype and that are apoptosis resistant, expand in patients with myocardial infarction (MI). MI patients harbouring high CD28null T cell numbers have increased risk of recurrent severe acute coronary events and unfavourable prognosis. The mechanisms that govern CD28null T cell expansion in MI remain elusive. The pro-inflammatory cytokine tumour necrosis factor-α (TNF-α) has been implicated in CD28null T cell expansion in rheumatoid arthritis. We investigated the effect of inflammatory and homeostatic cytokines on CD28null T cells in MI patients.

Danger-recognizing proteins, β-defensin-128 and histatin-3, as potential biomarkers of recurrent coronary events.

Conventional risk factors have limited ability to predict recurrent events in subjects with first-time coronary artery disease(CAD). This aim of this study was to identify novel biomarkers using comparative global proteome analysis to improve the risk assessment for recurrent coronary events. We used samples from phase-I of the Indian Atherosclerosis Research Study(IARS), consisting of 2,332subjects, of whom 772were CAD-affected subjects, including 152with recurrent events identified during a 5-year follow-up period. Global proteome analysis was performed on serum samples of 85subjects with recurrent coronary events and 85age- and gender-matched subjects with first-time CAD using surface-enhanced laser desorption ionization time-of-flight mass spectrometry with CM10 arrays. TagIdent was used for protein identification followed by validation by western blot analysis and ELISA. Data were analyzed by logistic analysis, Cox-regression, hazards ratio, C-statistics and combined-marker risk score using SPSS version-17 and R-package version-2.13.0 software. We identified 16significantly differentially expressed protein peaks. Of these, 2peaks corresponding to m/z8588 and1864 were identified as β-defensin-128 and histatin-3, belonging to the danger-recognizing peptide family, which exhibited a significant independent association with recurrent events(odds ratios of7.49 and1.4, respectively). C-statistics improved significantly from 0.677 for conventional risk factors alone to 0.800(p-value=0.001) in combination with β-defensin-128 and histatin-3 with a hazards ratio of1.833. A combined risk score of β-defensin-128 and histatin-3 could reclassify 112out of the 170subjects into intermediate- and high-risk groups. On the whole, our data indicate that β-defensin-128 and histatin-3 may be potential biomarkers whch may be used to improve risk the stratification for recurrent coronary events.

Planning secondary prevention: Room for improvement.

The prognosis of patients after acute coronary syndromes is still suboptimal, mainly due to the risk of recurrent adverse coronary events, which is greatest during the first year, but persists over one's lifetime. Meaningful progress in preventing cardiovascular events has been achieved. However, there remains much room for improvement by embracing innovative therapies and investing in multidisciplinary approaches. Pharmacological interventions focused on optimising antithrombotic and lipid-lowering therapies are both pillars of secondary prevention that have seen recent ground-breaking advances. Moreover, new approaches in diabetic patients with cardiovascular disease and new targets for anti-inflammatory treatment may significantly improve prevention strategies in the future. However, pharmacological treatments are expensive and can have significant side effects. Developing better tools in order to identify high-risk patients and promote more personalised strategies for each patient should be an absolute priority. Furthermore, adherence to medication is still low and represents a real challenge; several strategies to improve low adherence to treatment are currently under discussion. Non-pharmacological interventions are also essential. Improving communication with patients and advanced surveillance for those secondary risk factors that may negatively impact prognosis are crucial. Encouraging multidisciplinary teams that work effectively to optimise all aspects of secondary prevention, including a cardiac rehabilitation programme, is the optimal approach. Current secondary prevention strategies and suggestions for areas of improvement are discussed in this manuscript. However, the question remains: will research in secondary prevention continue to focus on stronger and more expensive drugs, or is it time for us to embrace a more patient-centred clinical and research model?

Terminalia methanol extracts inhibit the amidolytic activity of human activated factor XII (Hageman factor)

The long‐term goal of this study is to develop the selective inhibitors of FXIIa based on traditional medicine, which might be safe, and effective. There are positive correlations between increased plasma FXIIa levels with coronary heart disease as well as increased risk of recurrent coronary events. Although they maintain a normal hemostasis, FXII knockout mice (FXII−/−) display defective arterial thrombus formation. In addition, FXII−/− mice are protected from development of cerebral ischemia and pulmonary embolism. Thus, inhibition of FXIIa would help prevent cardiovascular diseases. The present study examines the effects of different but related herbal medicines that impact on the plasma blood coagulation FXII. While it initiates the activation of blood coagulation to stop any bleeding, FXII helps the remaining blood clotting factors and platelets to keep certain circulating pathogenic microorganism close to the phagocytes. The negative charge on the microorganism surface or platelet polyphosphate (poly P) binds readily to zymogen FXII, resulting in the activation of FXII. Evidence indicates that poly P containing pathogens promote FXII‐mediated blood coagulation independent of factor XI, reflecting a novel poly P‐induced thrombus formation. The methanol extracts of T. chebula fruit, T. bellirica fruit, T. arjuna fruit, and T. arjuna bark blocked FXIIa activity with IC50 values of 30, 50, 190, 190 and 27 mg/ml, respectively. Two isolated compounds from Terminalia, Arjunoglucoside II and arjunic acid blocked FXIIa activity with IC50 values of 370 and 780 μM, respectively. T. chebula fruit, T. and arjuna fruit extracts at 50 mg/ml did not affect endothelial cells viability. Overall, T. chebula fruit and T. arjuna fruit extracts might be useful to improve symptoms of FXIIa‐dependent inflammation and thrombosis.

Identification of vascular patients at very high risk for recurrent cardiovascular events: validation of the current ACC/AHA very high risk criteria.

To validate and assess performance of the current ACC/AHA very high risk criteria in patients with clinically manifest arterial disease. Data were used from the SMART study (n = 7216) and REACH Registry (n = 48322), two prospective cohorts of patients with manifest atherosclerotic arterial disease. Prevalence and incidence rates of recurrent major adverse cardiovascular events (MACE) were calculated, according to the ACC/AHA VHR criteria (cardiovascular disease combined with diabetes, smoking, dyslipidaemia, and/or recent recurrent coronary events). Performance of the ACC/AHA criteria was compared with single very high risk factors in terms of C-statistics and Net Reclassification Index. All patients were at VHR according to the ESC guidelines (incidence of recurrent MACE in SMART was 2.4/100PY, with 95% CI 2.3-2.5/100PY and in REACH 5.1/100PY with 95% CI 5.0-5.3/100PY). In SMART 57% of the patients were at VHR according to the ACC/AHA criteria (incidence of recurrent MACE 2.7/100PY, 95% CI 2.5-2.9/100PY) and in REACH this was 64% (5.9/100PY, 95% CI 5.7-6.1/100PY). The C-statistic for the ACC/AHA VHR criteria was 0.53 in REACH and 0.54 in SMART. Very high risk factors with comparable or slightly better performance were eGFR < 45, polyvascular disease and age >70 years. Around two third of the patients meeting the ACC/AHA VHR criteria had a predicted 10-year risk of recurrent MACE <30%. The ACC/AHA VHR criteria have limited discriminative power. Identifying patients with clinically manifest arterial disease at VHR for recurrent vascular events using eGFR <45, polyvascular disease, or age >70 years performs as well as the ACC/AHA VHR criteria.

POPULATIONAL STUDY OF LONG TERM OUTCOMES OF ACUTE MYOCARDIAL INFARCTION IN TOMSK

Aim. To evaluate long term outcomes of acute myocardial infarction (MI), based on the populational registry. Material and methods. In the study, the survived post-MI patients were included, in the year 2007 registered in database of MI (n=439). Prospective observation was done during 5 years after index event. In the case of fatal outcome the protocols were analyzed, of pathology studies and summaries of forensic autopsies; relatives were interviewed and the witnesses of clinical cases. For statistics, the software “Statistiсa” V.10 was applied. Results. Mortality among patients included into the study, was 11% in one year post MI, and 35% at 5 years. In overall structure of the causes of fatal outcomes there were cases of second MI — 37%. Chronic coronary heart disease was found as a cause of death in 21%, and in 2% there was fatal stroke; in 5% pulmonary embolism, and in 5% sudden cardiac death. In 17% causes of death were not related to cardiovascular pathology. Conclusion. Patients after MI do demonstrate high level of mortality in 5 year outcomes. Leading causes of fatal outcomes during first 2 years are recurrent acute coronary events, acute strokes, thromboembolism.

Factors affecting effective patient management for preventing recurrent coronary events

To identify factors affecting effective management of patients with myocardial infarction for preventing recurrent coronary events in the outpatient setting. The study group consisted of patients (n=111) with recurrent myocardial infarction. The control group consisted of patients with primary myocardial infarction (n=89) after percutaneous coronary intervention. Social and demographic, clinical and behavioral factors (weight loss, smoking cessation, adherence to therapy, physical and psychological rehabilitation) were evaluated. Risk factors contributing to the development of repeated MI were as follows: patients' age, concomitant polyvascular and multivessel disease, arterial hypertension, hypercholesterolemia, excess weight and smoking, poor adherence to the recommendations of cardiologists and general physicians. The analysis of the effectiveness of the management of patients with myocardial infarction demonstrated the importance of the outpatient rehabilitation in preventing repeated acute coronary events.

SMOKING AS A RISK FACTOR OF CARDIOVASCULAR AND CEREBROVASCULAR DISEASES: PREVALENCE, IMPACT ON PROGNOSIS, POSSIBLE SMOKING CESSATION STRATEGIES AND THEIR EFFECTIVENESS. Part 1. Smoking Prevalence and Impact on Prognosis

The prevalence of smoking in the Russian Federation is 27.7%. Losses of potential years of life in working age associated with premature death due to smoking in Russia on average are 9 years for men, for women – 5.6 years. Tobacco use is a risk factor for 6 of 8 main causes of death in the world: ischemic heart disease (IHD); cerebral circulation disorders; lower respiratory tract infection; chronic obstructive pulmonary disease; tuberculosis; trachea, bronchus, and lung cancer. The risk of developing IHD in smoking patients is increased by 2-4 times in men and women and in any age group. Myocardial infarction occurs in smoking patients at a younger age, and they have a similar risk of coronary events with patients of older age groups. The increased risk of recurrent coronary events persists with the continuation of smoking in the patient after myocardial infarction. Smoking is associated with a double risk of ischemic stroke and a 2-4-fold increase in the risk of subarachnoid hemorrhage. The risk of peripheral arteries diseases in smokers is increased 3-6 times than this in non-smokers. The mechanisms of development of acute cardiovascular events during smoking include the activation of inflammation, platelet aggregation/thrombogenesis, the sympathetic nervous system, and the development of endothelial dysfunction due to exposure to tobacco smoke components.

THE INFLUENCE OF CELL AND PLASMA HEMOSTASIS AND BIOMARKER LEVELS ON CLINICAL OUTCOMES IN PATIENTS WITH UNSTABLE ANGINA AND RESISTANCE TO ANTIPLATELET AGENTS

SUMMARY Objective: to assess the impact of cell plasma hemostasis disorders and the level of biomarkers on clinical outcomes and to develop laboratory diagnostic criteria forecast recurrent coronary events in patients with unstable angina. Material and Methods: the study included 124 patients with unstable angina. All patients were performed: complete blood count, to determine the level for TnI, the determination of inflammatory markers (hs C-reactive protein (CRP)), the level of myeloperoxidase, von Willebrand factor, the level of thrombin, fibrinogen (FG), antithrombin III (AT III), D-dimer, factor Xa), agregatogramm was performed an impedance aggregometer Multiplate and determining platelet activation by flow cytometry. All patients underwent ECG, echocardiogram, 24-hour ECG monitoring, coronary angiography. Results: developed independent predictors of the risk of recurrent coronary events in patients with unstable angina: the threshold values for evaluating platelet aggregation analyzer Multiplate-ASPI-test (AUC) &gt;52 U, ADP-test (AUC) &gt;60 U; the peak concentration of thrombin &gt;294,5 nM, platelet size - MPV &gt;9,6 fl, myeloperoxidase level &gt;316 pmol/l, hsCRP &gt;3.8 g/l, and troponin I &gt;0,07 ng/ml. We created the scale of the prediction of recurrent coronary events after suffering unstable angina. In patients included to the study it was found that 18 patients (14.5%) recorded a decrease of sensitivity to aspirin (ASA)in the standard dose of 75 mg, in 24 patients (19.4%) to clopidogrel 75 mg and in 8 patients (6,5%) - both to ASA and clopidogrel. It was found that the resistance to ASA and/or clopidogrel more than 2.5 [CI, 2.0; 2.8] once increases the relative risk of recurrent ischemic events. Conclusions: developed by independent predictors of the risk of recurrent coronary events in patients with unstable angina: AUC ASPI- test&gt;52 U, AUC ADP- test&gt;60 U; the peak concentration of thrombin&gt;294,5 nM, platelet size - MPV&gt;9,6 fl, myeloperoxidase &gt;316 pmol/l, high-sensitivity CRP &gt;3.8 g/l, the level of troponin I&gt;0,07 ng/ml. Keywords: unstable angina, resistance to ап^рШеШ agents, agregatogramm, cell and plasma hemostasis

Inflammatory markers modify the risk of recurrent coronary events associated with apolipoprotein A-I in postinfarction patients

Laboratory findings have suggested that systemic and vascular inflammation can impair the antiatherogenic function of high-density lipoproteins (HDLs). However, evidence from population studies is sparse. The objective of the study was to assess if blood inflammatory markers modify the risk of recurrent coronary events associated with apolipoprotein A-I (apoA-I) and HDL cholesterol (HDL-C) among postinfarction patients. ApoA-I, HDL-C, and inflammatory markers (C-reactive protein [CRP], serum amyloid A (SAA), fibrinogen, von Willebrand factor [vWF], and D-dimer) were measured from blood samples of 1028 patients drawn 2months after an index myocardial infarction (MI). Patients were followed up for the composite coronary endpoint (nonfatal MI, coronary death, or unstable angina) for an average of 26months. Cox proportional hazard models were used to assess effect modifications for the association of apoA-I and HDL-C with coronary risk by each inflammatory marker. CRP significantly modified the risk of recurrent coronary events associated with apoA-I. Among the entire population, multivariable-adjusted hazard ratios associated with each standard deviation increase in apoA-I for those with low and high CRP levels were 0.89 and 1.35, respectively (P value for interaction=.008). vWF was a significant effect modifier of the apoA-I/coronary risk association only among diabetic patients (hazard ratios were 0.56 and 1.43, for diabetic patients with low and high vWF levels, respectively; P value for interaction=.002). No effect modification was observed for the HDL-C/coronary risk association. Among stable post-MI patients, CRP modified the risk of recurrent coronary events associated with apoA-I. VWF modified this association only among the diabetic subgroup.

Effects of nutrition education on recurrent coronary events after percutaneous coronary intervention: A randomized clinical trial

Changes in lifestyle include a healthy diet. However, due to different educational approaches, the effects of nutritional counselling are still not very encouraging and require further study. The objective of this study was to analyse the effectiveness of a nutrition education intervention program on mortality and recurrence of cardiovascular events evaluated after one and four years of follow-up. A randomized clinical trial was performed at a public hospital in Brazil with 200 patients who had recently undergone elective percutaneous coronary intervention (PCI). In addition to the traditional care, the patients allocated to the intervention group attended nutrition education workshops that adopted a constructivist approach towards behavioural change for six months. Primary outcome was death, and secondary outcomes were acute myocardial infarction (AMI), revascularization with re-PCI, or coronary artery bypass graft (CABG) surgery. The magnitude of the first year effect was calculated by the absolute risk reduction, and the risk ratio was calculated as a measure of the cumulative incidence of events after four years. The critical p-value was assumed as 5%. After one year of follow-up, in the intervention and control groups, respectively, there were 5 and 7 deaths (p = 0.53); 5 and 6 AMIs (p = 0.73); 4 and 6 re-PCIs (p = 0.50); and 4 and 4 CABGs (p = 0.98). After four years, the risk ratios between intervention and control groups were 0.75 (95% CI 0.35–1.58) for death, 0.89 (95% CI 0.34–2.28) for AMI, 0.86 (95% CI 0.40–1.84) for re-PCI, and 1.14 (95% CI 0.38–3.40) for CABG. Although differences in events between the two groups were not significant, data suggest that the lower number of events observed in the intervention group is most notable with the longer follow-up. NCT01028066 . Registered 8 December 2009, retrospectively registered.

The fundamental importance of smoking cessation in those with premature ST-segment elevation acute myocardial infarction.

Smoking is the most prevalent risk factor among young patients suffering acute myocardial infarction (AMI). In this review, we will present data on the detrimental consequences of continued smoking with regard to the recurrence of coronary events after an AMI at an early age. A prospective study with long-term follow-up of young survivors of AMI showed that continuation of smoking after a first episode of AMI was the strongest independent predictor of further cardiac events. In particular, persistent smokers had ∼2.5 times higher risk of a new coronary event when compared with nonsmokers. This emphasizes the fundamental importance of initiating smoking cessation treatment in all smokers with AMI during hospitalization. Extrapolating the results of previous studies showing the benefits of smoking cessation in middle-aged or elderly coronary patients, an even greater benefit should be expected in young patients because of their specific characteristics, which are presented in the current review. Young persistent smokers after a premature AMI constitute a high-risk subgroup for a recurrence of cardiac events. Therefore, smoking cessation is a key issue for improving their prognosis and all smokers should be offered effective antismoking treatment at the time of initial hospitalization.

LATITUDE-TIMI: is there still hope for anti-inflammatory therapy in acute myocardial infaction?

Inflammation is a crucial feature of atherosclerotic plaque formation as well as post myocardial infarction (MI) remodeling and thus thought to play an essential role in the pathogenesis of ischemic heart disease and its complications (1,2). The regenerative processes after MI involve inflammatory, proliferative and maturation phases that are crucial for wound healing and reparation (3). However, an overactive inflammatory and fibrotic response is associated with maladaptive structural and electrophysiological remodeling, leading to systolic as well as diastolic dysfunction and contributing to the development of an arrhythmogenic substrate (2,4). Moreover, elevated cytokine levels also correlate with increased risk for recurrent coronary events in patients with MI (5).

Lipoprotein(a) level as a predictor of long-term cardiovascular outcomes after percutaneous coronary interventions

Objectives: To evaluate the relationship of lipoprotein(a) [Lp(a)] concentration to recurrent coronary events after coronary artery percutaneous coronary interventions (PCI).

Economic evaluation of exercise-based cardiac rehabilitation in patients with a recent acute coronary syndrome.

Health care decision-making requires evidence of the cost-effectiveness of medical therapies. We evaluated the cost-effectiveness of exercise-based cardiac rehabilitation (ECR) implemented according to guidelines. All the patients (n=204) had experienced a recent acute coronary syndrome and were randomized to a 1-year ECR (n=109) or usual care (UC) group (n=95). The patients' health-related quality of life was followed using the 15D instrument and health care costs were collected from electronic health registries. The cost-effectiveness of ECR was estimated based on intervention and health care costs and quality-adjusted life years (QALYs) gained. The total average cost per patient was lower in ECR than in UC. The incremental cost was divided by the baseline-adjusted incremental QALYs (0.045), yielding an incremental cost-effectiveness ratio of -€24511/QALYs. A combined endpoint of mortality, recurrent coronary event, or hospitalization for a heart failure occurred for five patients in ECR and 16 patients in UC (HR 3.9, 95% CI 1.4-10.6, P=0.004, relative risk reduction 73%, number needed to treat eight). ECR is a dominant treatment option and decreases the occurrence of adverse cardiac events. These results are useful for decision-making when planning optimal utilization of resources in Finnish health care.